Broadly stated, this research project has two goals. First, I plan to investigate behavioral, neurophysiological, and neurochemical aspects of analgesia produced by focal electrical stimulation of the brain, to compare this phenomenon to analgesia produced by morphine micro-injection, and to examine the relationship of these phenomena to the more general problem of the neural and neurochemical basis of narcotic addiction. Some of the specific goals subsumed under this project include: 1) To precisely describe the neuroanatomical pathways utilized and the ultimate sites and mechanisms of analgesic action 2) To examine behavioral manifestations of tolerance and physical dependence to the analgesia produced by these procedures and to relate these findings to the general problem of opiate addiction. 3) To characterize physiologically and pharmacologically the neural population responsible for analgesia, and to relate this population to neural populations underlying other stimulation-elicited behaviors. 4) To be able to suggest new and practical treatment procedures for difficult or intractable pain syndromes in man. Secondly, I propose to identify, employing electrophysiological techniques, brain areas with behaviorally significant involvement in pain perception. Stimulation-produced analgesia, morphine analgesia, and behavioral manipulation of pain perception will be utilized as tools to achieve this goal. BIBLIOGRAPHIC REFERENCES: Akil, H., Mayer, D. J. and Liebeskind, J. C. Antagonism of stimulation-produced analgesia by naloxone, a narcotic antagonist. Science, 1976, 191, 961-962. Hayes, R. L., Newlon, P. G., Rosecrans, J. A. and Mayer, D. J. Reduction of stimulation-produced analgesia by lysergic acid diethylamide, a depressor of serotonergic neural activity. Brain Res., 1977, 122, 367-372.